Findings of study show some heart attack patients may actually benefit from mild to moderate sleep-disordered breathing.

Doctors have for years warned people suffering from sleep apnea – where they
awaken momentarily dozens or even hundreds of times per night – to lose weight
and wear so-called continuous positive airway devices on their noses to increase
their oxygen supply and reduce their resultant risk for cardiovascular
disease.

But a counterintuitive study conducted at the Technion- Israel
Institute of Technology in Haifa suggests that some heart attack patients may
actually benefit from mild to moderate sleep-disordered breathing.

Apnea
and other types of sleep-disordered breathing can boost the numbers and
functions of rare cells that help repair and build new blood vessels, according
to cell biologist Dr. Lena Lavie, her husband, Prof. Peretz Lavie (president of
the Technion and a well-known sleep medicine expert), and their Technion
colleagues, Dr. Slava Berger and Prof. Doron Aronson.

They say the
findings could help predict which patients are at a greater health risk after a
heart attack and might even suggest ways to rebuild damaged heart
tissue.

Their study was just published in the American Journal of
Respiratory and Critical Care Medicine and was accompanied by an editorial
written by Dr. Leila Kheirandish-Gozal of the University of Chicago and Prof.
Ramon Farré of the University of Barcelona in Spain.

Sleep-disordered
breathing is characterized by cycles of apnea-induced hypoxia in which the
sleeper experiences a temporary drop in oxygen levels. Between five percent and
10% of the general adult population suffers from it, but it is much more common
– 40% to 60% – among cardiac patients.

Many studies have shown that sleep
apnea is a risk factor for everything from high blood pressure to chronic heart
failure, Lena Lavie noted. Earlier studies by the Haifa scientists suggest apnea
increases oxygen-related stress and inflammation in the heart and blood
vessels.

The study could help resolve a puzzling medical issue. If sleep
disordered breathing is associated with cardiovascular disease, why is it that
people who suffer from breathing disorders in sleep seem to do as well as
healthy sleepers after a heart attack?

The Technion researchers examined 40 male
patients – a mix of healthy sleepers who served as a control group and others
with sleep disordered breathing who had had a heart attack just a few days
earlier. Blood samples revealed that the sleep-disordered- breathing heart
patients had markedly higher levels of endothelial progenitor cells (EPCs),
which give rise to new blood vessels and repair the injured heart. They also had
higher levels of other growth-promoting proteins and immune cells that stimulate
blood vessel production.

The researchers were able to trigger a similar
increase in vessel-building activity in vascular cells taken from a second set
of 12 healthy men and women by withholding oxygen from the cells for short
periods.

“Indeed, our results point to the possibility that inducing
mild-moderate intermittent hypoxia may have beneficial effects,” Lena Lavie
said.

The Spanish authors of the accompanying editorial in the journal
said the Technion study moved toward reconciling the ideas that apnea can stress
the heart but also “precondition” it for repair.

Patients with
sleep-disordered breathing, they noted, “are essentially better prepared to
harness the recruitment of EPCs when [a heart attack] comes knocking at the
door.”

According to Aronson, who is also affiliated with Haifa’s Rambam
Medical Center, a heart attack is a “potent stimulus for EPC
mobilization.”

He also explained that the cells move from bone marrow to
the heart to repair damaged tissue after a heart attack.

“The field of
cell-based cardiac repair has struggled to find the best approach to enhance
recruitment of EPCs to the heart following myocardial infarction,” he said. The
Technion findings, he added, suggest that intermittent periods of oxygen
deprivation in heart attack patients “provides a simple and powerful means to
boost EPC mobilization.”

According to Lena Lavie, it should be “further
investigated if inducing intermittent hypoxia immediately after a heart attack,
in patients without sleep disordered breathing, will also have such an
effect.”

The researchers hope to test this possibility in animal studies,
as well as expand their studies of the underlying mechanisms that activate EPCs
and other vessel-building factors.